caa a22 4500 477120660 CHVBK 20180405111636.0 cr unu---uuuuu 170330e19960301xx s 000 0 eng 10.1007/BF00408637 doi (NATIONALLICENCE)springer-10.1007/BF00408637 Calcium channels and cation transport ATPases in cardiac hypertrophy induced by aortic constriction in newborn rats [Elektronische Daten] [Lei Zheng, Maurice Wibo, Frantisek Kolář, Théophile Godfraind] Cardiac enlargement due to gradual pressure overload was induced by abdominal aortic constriction in 2-day-old rats. On day 90, the functional performance of the left ventricle was assessed by acute load test (ligation of ascending aorta) in open-chest anaesthetized animals. Two subgroups, designated compensated and decompensated hypertrophy (CH and DH), were distinguished on the basis of the functional reserve of left ventricle, which was significantly impaired in DH but not in CH, and of right ventricle weight, which was markedly increased in DH but not significantly modified in CH. In total particulate fractions prepared from hypertrophied left ventricles, the levels (per g tissue) of sarcoplasmic reticulum Ca2+-transport systems were decreased, either slightly (by 13-16%: [3H]ryanodine binding) or moderately (by 28%: thapsigargin-sensitive Ca2+-ATPase activity). The number of sarcolemmal L-type Ca2+ channels ([3H]PN200-110 binding) was not modified significantly, while that of β1-adrenoceptors ([3H]CGP-12177 binding) was reduced, especially in the DH group (by 39%). Na+,K+-ATPase activity was reduced by 28% in CH and 41% in DH. [3H]Ouabain binding experiments (saturation and dissociation) indicated the existence of two high-affinity binding sites, attributable to the Na+,K+-ATPase α3 and α2 subunit isoforms; while the relatively minor α3 component did not change significantly in hypertrophied ventricles, the α2 component was markedly down-regulated, decreasing by 57% in CH and 82% in DH. Kluwer Academic Publishers, 1996 Ca2+ channel nationallicence ryanodine nationallicence β-adrenoceptor nationallicence Na+,K+-ATPase nationallicence Ca2+-ATPase nationallicence cardiac hypertrophy nationallicence Zheng Lei Laboratoire de Pharmacologie, Université Catholique de Louvain, B-1200, Brussels, Belgium aut Wibo Maurice Laboratoire de Pharmacologie, Université Catholique de Louvain, B-1200, Brussels, Belgium aut Kolář Frantisek Institute of Physiology, Academy of Sciences of the Czech Republic, CZ-142 20, Prague, Czech Republic aut Godfraind Théophile Laboratoire de Pharmacologie, Université Catholique de Louvain, B-1200, Brussels, Belgium aut Molecular and Cellular Biochemistry Kluwer Academic Publishers; http://www.wkap.nl 163-164/1(1996-03-01), 23-29 0300-8177 163-164:1<23 1996 163-164 11010 https://doi.org/10.1007/BF00408637 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00408637 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Zheng Lei Laboratoire de Pharmacologie, Université Catholique de Louvain, B-1200, Brussels, Belgium aut NATIONALLICENCE 700 1- Wibo Maurice Laboratoire de Pharmacologie, Université Catholique de Louvain, B-1200, Brussels, Belgium aut NATIONALLICENCE 700 1- Kolář Frantisek Institute of Physiology, Academy of Sciences of the Czech Republic, CZ-142 20, Prague, Czech Republic aut NATIONALLICENCE 700 1- Godfraind Théophile Laboratoire de Pharmacologie, Université Catholique de Louvain, B-1200, Brussels, Belgium aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Kluwer Academic Publishers; http://www.wkap.nl 163-164/1(1996-03-01), 23-29 0300-8177 163-164:1<23 1996 163-164 11010 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer